Introduction. We sought to investigate whether there was a difference between cyclosporine (CsA) and mycophenolate mofetil (MMF) to affect the expression of Fractalkine/ CX3CR1 in chronic allograft nephropathy (CAN). Methods. The Sprague-Dawley Wistar rat accelerated kidney sclerosis model was performed as modified from the procedure of Kamada. Recipients were divided into three oral treatment groups (each group n=8): group A was CsA 10mg/kg•d for 10 days followed by vehicle; group B was CsA 10mg/kg•d for 10 days followed by CsA 6mg/kg•d; group C was CsA 10mg/kg•d for 10 days followed by MMF 20mg/kg•d. Pathological changes graded according to Banff 97 Standards were observed at 4, 8, and 12 weeks posttransplantation. The immunohistochemistry and quantitative real-time fluorescence polymerase chain reaction (PCR) were used to assess the distribution and expression of Fractalkine/CX3CR1 in the grafted kidney. Results. Fractalkine/CX3CR1 were mostly expressed in the tubulointerstitium and tubular epithelial cell basolateral membrane. A proportion of the vessel showed positive staining for Fractalkine/CX3CR1, occasionally in glomerular parietal wall cells. The expression of Fractalkine/CX3CR1 in grafted kidneys at all the time points was significantly less in the MMF than in the CsA group or the control group (P<.05). Real-time fluorescence quantitative PCR revealed similar outcomes as immunohistochemistry. The expression of Fractalkine coincided with CX3CR1. Conclusion. Fractalkine/CX3CR1 may play an important role in the development of interstitial fibrosis in CAN. Different immunosuppresants have various effects on expression of the Fractalkine/CX3CR1.

Aim. Serum cystatin C (SCysC) has been proposed as a better marker of glomerular filtration rate (GFR) than serum creatinine (Scr). However, few data are available in renal transplant patients, especially, during the early postoperative phase. Methods. Thirty-nine renal transplant patients (22 men/17 women) were recruited for determination of SCysC and Scr before operation, at 1 week and at 4 weeks after operation. SCysC was determined by particle-enhanced turbidimetric immunoassay. Creatinine clearance (Ccr) was calculated using the Cockcroft-Gault formula. Results. SCysC and Scr levels significantly decreased with the recovery of allograft function. SCysC showed a significant correlation with Scr and Ccr. The relationship between SCysC and Scr showed a positive correlation (r=.849 preoperation, and r=.940 postoperation). The relationship between SCysC and Ccr revealed a negative correlation (r=.857 preoperation, and r=.876 postoperation). At the Ccr level of 50 to 80mL/min/1.73m2, the correlation between SCysC and Ccr (r=.778) was significantly better than that between Scr and Ccr (r=.553; P=.032). The concentration of SCysC was not affected by age, gender, height, body weight, hemoglobin, serum protein, glucose, or mycophenolate mofetil or azathioprine dosage. However, corticosteroids slightly increased the level of SCysC and cyclosporine (CsA) decreased it. The area under the curve of the receiver operating characteristic curve for SCysC and Scr are 0.964 and 0.915, respectively (P<.05). Conclusion. Although the concentration may be slightly influenced by prednisolone and CsA, SCysC is more sensitive than Scr to detect early and moderate deterioration of GFR in adult renal transplant recipients.

ORGAN transplantation has become a realistic treatment for patients with end-stage organ failure.1,2 However, despite improvements in diagnosis and treatment of acute rejection, the consequences of chronic rejection, namely transplant arteriosclerosis, remain major obstacles to long-term survival of most solid organ allografts.3,4 Several animal models have been developed to investigate the mechanisms of the chronic rejection.5-7 However, most of these models have the disadvantages of requiring difficult operative skills, ensuring high rates of postoperative complications and host mortality as well as requiring a long time of observation. The present study was designed to investigate the feasibility of using SD and Wistar rats to design a new rat model of transplant arteriosclerosis and to accelerate the process by enhancing the ishemia/reperfusion (IR) injury.